What is your personal theory or understanding of ME/CFS?

femtosecond99

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In my view this is a common deficit in psych arguments because they fall into that whole nest of nasties associated with Cartesian Dualism. These deficits, in my experience, have elements in common with religionists.
Ah, I think that may be the problem. Cartesian Dualism doesn't exist, and no sane scientist espouses it any more. I think the problem is many people still cling on to the belief that the mind and body are completely separate, even though that idea has been thoroughly debunked.
 

cmt12

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In my view this is a common deficit in psych arguments because they fall into that whole nest of nasties associated with Cartesian Dualism. These deficits, in my experience, have elements in common with religionists.
A valid concern but..

I suggest you look at the objective indicators, and remove yourself as much as possible from subjective vantages.
In my view, the anti psych materialist naively ignores or underestimates the difficulty of removing bias and distortion (subjectivity). They believe their judgments to be logical (objective) conclusions that follow empirical data when it reality they are using intuition and affected by confirmation bias as well.
 

Hip

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Later work by those scientists showed that the same viruses are present in healthy people:
The fact that the same non-cytolytic enterovirus infection is also found in the muscles of healthy people was known even in their earliest work. But the prevalence of these muscle infections was much higher in ME/CFS patients.

That's normally what you demonstrate in pathogen studies: you show that the pathogen is much more prevalent in the disease patients than in the healthy controls. In that way, you prove an association. Of course proving whether or not the pathogen actually causes the disease requires more research.

But there is nothing in the enterovirus muscle infection research that disproves the possibility that this virus may cause ME/CFS.

There is also the enterovirus brain infection research, which so far shows complete 100% correlation between the presence of the infection and ME/CFS.



That's not quite true. Cortisol doesn't turn down the immune system, it shifts it from Th1 (intracellular) to Th2 (extracellular) response.
You are right, it's just the Th1 response cortisol reduces, which results in a Th2 boost.



The results were not statistically significant.
The study's conclusion that responders were 7.4 times more likely to be in the Valcyte group was a statistically significant finding (p-value = 0.029).

But the limitations of the Montoya study were the small amount of patients, and the very short treatment time of only 6 months. Lerner's study indicates that improvement is gradual, and takes 3 months for the benefits to begin to appear, and around 2 years for the full benefits to manifest, with not much further improvement being made after the 2 year point.

You can see the gradual improvements in Table 3 of Lerner's study, which I copied into this post.



It could also have been that the treatment had no effect, and both groups gradually improved but the more ill group just took longer to improve.
That's a possibility, but if you look at studies which have examined the improvement and recovery rate of ME/CFS patients, in the general case they show that improvement and recovery is rare (see this study which found improvement in less than 6% of patients after 5 years).

So the improvements in Lerner's patients seem unlikely to be due to natural improvement, because it seems there is rarely natural improvement in ME/CFS in general.

However, for the post mononucleosis ME/CFS subset, recovery looks much more common: this study found that at first contact, 10% of patients were still working, but after 7 years, 55% were at work.

So post-mono ME/CFS seems to have a far more optimistic prognosis than ME/CFS in the general case (ME/CFS linked to other viral or non-triggers).

Maybe EBV-linked ME/CFS is just "ME/CFS lite" compared to the ME/CFS associated with other viruses?
 
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duncan

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In my view, the anti psych materialist naively ignores or underestimates the difficulty of removing bias and distortion (subjectivity). They believe their judgments to be logical (objective) conclusions that follow empirical data when it reality they are using intuition and affected by confirmation bias as well.
I am speaking to objective evidence as defined and embraced by even the IDSA/CDC/NIH.

There is plenty of data from plenty of patients that support active infections.

Nothing naive involved, and no amount of psych consults can dispute the conformity to IDSA doctrine for these Bb patients who present with symptoms AND labs post-standard IDSA protocol..
 

femtosecond99

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There is also the enterovirus brain infection research, which so far shows complete 100% correlation between the presence of the infection and ME/CFS.
As far as I'm aware, it is just one post-mortem that found enterovirus DNA. And as you point out above, that is also found in healthy controls. I think if there was any possibility that it was causing CFS, OMF and others would be looking into it.
 

JES

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In my view, the anti psych materialist naively ignores or underestimates the difficulty of removing bias and distortion (subjectivity). They believe their judgments to be logical (objective) conclusions that follow empirical data when it reality they are using intuition and affected by confirmation bias as well.
Well it's perhaps too obvious to repeat, but drug trials already have a standard by which to remove bias. The most common way to do this by double blinded study, which has a placebo group and an active drug group, which are blinded both from the patients and the study conductors.

Unfortunately, it seems to be that psychiatric trials rarely follow the same standard. The PACE trial for example, which was supposed to be the biggest and best, had no blinding, so patients knew exactly what therapy they were going to get in advance, and what's worse, the therapies that were preferred by the investigators (CBT/GET) were actively promoted by leaflets to be effective. The lack of blinding and relying on subjective improvement criteria only, as in the PACE trial, is a major problem and it seems to me that some kind of bias is almost inbuilt in this sort of trial, whereas drug trials at least follow the standard of blinding.
 

cmt12

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I am speaking to objective evidence as defined and embraced by even the IDSA/CDC/NIH.

There is plenty of data from plenty of patients that support active infections.

Nothing naive involved, and no amount of psych consults can dispute the conformity to IDSA doctrine for these Bb patients who present with symptoms AND labs post-standard IDSA protocol..
The issue is causation. There is a leap, a gap, from observation to a theory of causation. In that gap exists bias, even for the “rational” scientist.

The question is who is more credible - someone who consistently warns to be aware of bias or someone who is insistent their theory is the right one but never brings up the possibility of bias, while assuming that anyone who disagrees with them is missing something.
 

duncan

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The question is who is more credible - someone who consistently warns to be aware of bias or someone who is insistent their theory is the right one but never brings up the possibility of bias, while assuming that anyone who disagrees with them is missing something.
Not for nothing, but your question lays the foundation for bias. :)

Everyone needs to be wary about bias. But the issue was one of bias based on - your words - "intuition" vs objective testing whose metrics are accepted by the most conservative of agencies. I am only advocating for the latter.

Moreover, I am suggesting that there are many diagnosed with ME/CFS who satisfy those metrics.
 
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Hip

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As far as I'm aware, it is just one post-mortem that found enterovirus DNA. And as you point out above, that is also found in healthy controls. I think if there was any possibility that it was causing CFS, OMF and others would be looking into it.
There are actually 3 post-mortem studies that found enterovirus RNA in the brain, Dr John Chia's being the latest one. They are detailed in this post.

The brains of 8 controls were also tested, and these were found to be enterovirus negative.


The Ron Davis and the OMF are going to test for enteroviruses and herpesviruses in their ME/CFS Severely Ill-BIG DATA Study. I just hope they understand that in ME/CFS you will not find much enterovirus in the blood, only in the tissues.
 

femtosecond99

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There are actually 3 post-mortem studies that found enterovirus RNA in the brain, Dr John Chia's being the latest one. They are detailed in this post.

The brains of 8 controls were also tested, and these were found to be enterovirus negative.


The Ron Davis and the OMF are going to test for enteroviruses and herpesviruses in their ME/CFS Severely Ill-BIG DATA Study. I just hope they understand that in ME/CFS you will not find much enterovirus in the blood, only in the tissues.
Kamaroff concluded:

"Some studies have found that enterovirus infection may be involved in CFS (68–72), but others have reported negative (73–75) or equivocal (76) results. Although one report claimed the discovery of a novel retrovirus in CFS (77), subsequent work has strongly challenged that claim (78–80)."

I think all we can do is await the results of further studies.
 

Hip

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Kamaroff concluded:

"Some studies have found that enterovirus infection may be involved in CFS (68–72), but others have reported negative (73–75) or equivocal (76) results. Although one report claimed the discovery of a novel retrovirus in CFS (77), subsequent work has strongly challenged that claim (78–80)."
Would you have a link or the title to that paper, I cannot find it. I'd like to read those negative studies.

I have not come across any negative enterovirus studies, apart from some work at the CDC, where they tried to detect enterovirus in ME/CFS using PCR on blood samples, and as you would expect, got negative results.
 

femtosecond99

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Would you have a link or the title to that paper, I cannot find it. I'd like to read those negative studies.

I have not come across any negative enterovirus studies, apart from some work at the CDC, where they tried to detect enterovirus in ME/CFS using PCR on blood samples, and as you would expect, got negative results.
It's this one:

https://www.ncbi.nlm.nih.gov/pubmed/9509246

Full-text is on sci-hub. It's pretty old, but then again I think most of those enterovirus studies are from the 90s.
 

Hip

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Thanks. The three negative papers mentioned in the above review you provide are give below. The second out of three used the wrong methods of detection, but it is not clear why the first and third failed to find enterovirus in ME/CFS patient muscles.

Failure to demonstrate enterovirus in Swedish patients with the chronic fatigue syndrome — 1996
(I could not find this exact title, but this paper I think refers to the same study results)

This study failed to find any enterovirus by PCR in muscle biopsies of 29 ME/CFS patients.

It's not clear why this study failed to find enterovirus, as muscle biopsies are exactly the right place to look for enterovirus in ME/CFS.

One possible explanation is the PCR primers used: their primer targeted the 5' region of the enterovirus genome — well this is the viral genome region where there are genetic deletions in non-cytolytic enteroviruses, so this might explain why the authors could not detect these viruses. (In non-cytolytic enterovirus, small parts of the enterovirus genome in the 5' region gets deleted and are no longer present; thus non-cytolytics do not carry to full enterovirus genome).

However, the other 7 studies that successfully found enterovirus in ME/CFS patients' muscles also used primers that target the 5' region, but perhaps it was a different part of that region?



Enteroviruses and the chronic fatigue syndrome — 1994

This study failed to find any difference between 76 ME/CFS patients and 76 healthy control in terms of detecting enterovirus, using:
  • Antibody blood tests by ELISA (now known to be unreliable for detecting chronic enterovirus)
  • Antibody blood tests by complement fixation testing (now known to be useless for detecting chronic enterovirus)
  • VP1 test of the blood (well you don't find much virus in the blood in ME/CFS, and I think this VP1 test developed by Prof Mowbray was shown ineffective)
  • Isolation of virus from stool specimens (this approach is not valid for finding non-cytolytic enteroviruses, to my knowledge anyway)
  • PCR on stool samples (this approach is not valid for finding non-cytolytic enteroviruses, to my knowledge anyway)
I don't think they employed any detection method that was likely to find chronic non-cytolytic enterovirus infections. To successful detect chronic non-cytolytic infections in ME/CFS, Dr Chia found you need to use antibody blood tests by neutralization (the gold standard of antibody detection), whereas ELISA, IFA or CFT are not reliable. Or you need to detect infections in tissue samples (eg gut or muscle tissues) by PCR or VP1 protein staining.



Investigation by polymerase chain reaction of enteroviral infection in patients with chronic fatigue syndrome — 1996

This study examined 34 muscle biopsies from ME/CFS patients and 10 muscle biopsies from controls. They used the same PCR primers as Gow (who found enterovirus in his study), so it cannot be a primer issue.

But commenting on the differences between their negative and Gow's positive results, the authors say:
The difference in findings between our study and that of Gow et al. [21] may be due to the population of CFS patients studied. Although the diagnostic criteria of both groups was broadly similar, the patients used in the study of Gow et al. [21] all reported that the illness had an acute onset after a feverish illness, whereas only 58% of patients in our study reported a viral infection before the onset of their illness.

Another possible explanation comes from the work of Galbraith et al. [24]. Direct sequencing of PCR products from enterovirus-positive serum samples of patients with CFS by these authors has suggested the presence of distinct novel enteroviruses. These viruses are thus unclassified and their site of replication is unknown. Thus, the different findings of different studies may reflect the nature of the samples examined.

Alternatively, it may be that these novel viruses replicate in non-muscle cells such as macrophages and that infiltration of damaged muscle by macrophages is a necessary prerequisite for the detection of viral presence.
So the authors suggest that there may have been more non-viral patients in their cohort. And different unknown and unclassified enteroviruses might be involved.
 
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halcyon

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The Swedish enterovirus study seems highly suspect to me. Ignoring the fact that it uses bogus criteria, it seems impossible that they found absolutely zero virus in anyone. As other valid studies showed, you should find some evidence of virus even in healthy controls. The fact that they found not a single person with virus makes me think their was something very wrong with their methodology.
 

wastwater

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MUM1/IRF4 is a deletion I likely harbour and is involved in T and B cells
Expression profile of MUM1/IRF4, BCL-6, and CD138/syndecan-1 defines novel histogenetic subsets of human immunodeficiency virus–related lymphomas

There was more interest in endogenous retroviruses eventually,I wonder if some of these integrated retroviruses might only be a few generations old rather than ancient
 
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There is also the enterovirus brain infection research, which so far shows complete 100% correlation between the presence of the infection and ME/CFS.
Where? Sorry this is interesting to me and not sure what you are referring to (paper link)?
 

Avenger

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Dear all,
I am not sure if this an answer to the correct thread but... I have something that is more than a theory...

I believe that there is the possibility of more than one form of Bacterial Overgrowth involved due to Gut dysbiosis and there is evidence for this. But there are a number of other factors involved....

Gut dysfunction, dysbiosis and Bacterial Overgrowth has been found in many ME/CFS (Sheedy et al found D-Lactic producing Bacteria in their CFS patients and came to the conclusion that Neurological symptoms found in ME/CFS and Mitochondrial dysfunction would be caused by the overproduction of D-Lactic acid).

I had been diagnosed with ME/CFS and even Fibromyalgia for 18 years of often severe illness, but have now been diagnosed with D-Lactic acidosis and now have my symptoms under controll simply using a diet that excludes Carbohydrates and Simple sugars (which will convert to D-Lactic acid if not excluded from my diet).

My belief is more than a theory; If IBS is caused by Bacterial Overgrowth (it can be controlled with antibiotics) and D-Lactic acidosis is a more severe form of Bacterial Overgrowth, then there may be a number of different forms of Bacterial Overgrowth including Fibromyalgia.

Bacterial Overgrowth does not properly describe what is essentially an infection which causes poisoning through the metabolites including D-Lactic acid produced by the Bacteria. Bacterial Overgrowth causing D-La is most certainly acting as an infection although it may remain in the Gut D-Lactic acid which cannot be metabolized can be found in spinal fluid to cause varying levels of neurological symptoms.

My own belief is that there are more than one combination of Overgrowth caused by different combinations of Bacteria that have (as in my own case) been made resistant to antibiotics which may have contributed to the different combinations of Overgrowth. Gut dysbiosis is an 'unexplored continent' (and Gut Bacteria are also subject to Viruses which can alter or modify their own DNA).

Different Antibiotics can select for Overgrowth in different ways through some Bacteria gaining resistance while other Bacterial Colonies are decimated to cause dysbiosis with remaining Overgrowths. I believe that the overuse of antibiotics in both medicine and agriculture (where our Bacteria are exposed to small quantities of Antibiotics that come from meat products and have caused Resistance of some Bacteria) have contributed to ME/CFS in at the very least a Subset.

I was forced to diagnose myself and when I was formally diagnosed with D-La without Short Bowel syndrome realized the implications. If I could have D-La without Short Bowel Syndrome then others could also.

My own belief is that the reason that ME/CFS patients with D-La have been left undiagnosed is that D-La was believed to be rare condition. Luke White 'D-Lactic acidosis more prevalent than we think' believes that it may be more common.

Causation may be extremely complex and there are other causes of Bacterial Overgrowth which is a very poor prognosis of health. Gastroenterologist Luke White also stated that anyone with Bacterial Overgrowth may be at risk of developing D-Lactic acidosis.

D-Lactic acidosis can also be a self perpetuating illness through the production of Methane which is known to cause slow motility/constipation and feeds back to perpetuate D-Lactic acidosis. This is all very complex and urgently needs research. Most medical investigations will be normal even with serious symptoms for D-La!

There may be several different combinations of Bacteria producing different metabolites. Fibromyalgia could be one of a number of variants of Bacterial Overgrowth, which to all intents and purposes acts as both infection and poisoning. D-La would explain fluctuating neurological symptoms expressed by ME patients for decades.

Paul.